Inflammatory Disease Mice

Inflammatory disease models include autoimmune models (rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis), inflammatory bowel disease models, asthma/allergy models, and tissue specific inflammation models. Models can use knockout, knockin, or conditional approaches to study inflammatory mechanisms.

Common Cre drivers include LysM-Cre (macrophages/neutrophils), CD4-Cre (T lymphocytes), CD11c-Cre (dendritic cells), CX3CR1-Cre (monocytes/macrophages), and tissue specific drivers (Villin-Cre for intestine, Keratin14-Cre for skin). Selection depends on whether you're studying immune cell contributions or tissue specific inflammatory responses.

Inflammatory phenotypes vary dramatically with genetic background. C57BL/6 shows Th1-biased responses; BALB/c shows Th2-biased responses. These differences affect disease severity, immune cell recruitment, and cytokine profiles. Consistent background use within studies is critical for reproducibility and interpretation.

Yes. Genetic modifications can be combined with environmental factors (DSS, TNBS, OVA, house dust mite, adjuvant) to model gene-environment interactions in inflammatory diseases. Conditional approaches enable study of how specific genes contribute to inflammatory responses in controlled challenge protocols.